A. Famurewa, Chima A. Ekeleme-Egedigwe, E. David, C. Eleazu, A. M. Folawiyo, N. Obasi
{"title":"Zinc abrogates anticancer drug tamoxifen-induced hepatotoxicity by suppressing redox imbalance, NO/iNOS/NF-ĸB signaling, and caspase-3-dependent apoptosis in female rats","authors":"A. Famurewa, Chima A. Ekeleme-Egedigwe, E. David, C. Eleazu, A. M. Folawiyo, N. Obasi","doi":"10.1080/15376516.2019.1669243","DOIUrl":"https://doi.org/10.1080/15376516.2019.1669243","url":null,"abstract":"Abstract Tamoxifen (TAM) is used in breast cancer chemotherapy since its approval by the Food and Drug Administration in 1977. However, TAM therapy is accompanied with hepatotoxicity – a source of worry to clinicians. Oxidative stress and inflammation are the major implicated mechanisms contributing to TAM hepatotoxicity. In this study, we explored whether zinc (Zn) supplementation could prevent TAM-induced hepatotoxicity in female Wistar rats. Rats were subjected to oral pretreatment of Zn (100 mg/kg body weight (b.w.)/day) for 14 days against hepatic toxicity induced by single intraperitoneal administration of TAM (50 mg/kg b.w.) on day 13. TAM markedly elevated serum liver enzymes, whereas total protein and albumin considerably reduced. TAM caused prominent depletion of hepatic-reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity. Also, TAM significantly increased malondialdehyde (MDA) level. Further, it raised liver levels of tumor necrosis factor-α (TNF-α), interleukin-1β, (IL-1β), interleukin-6 (IL-6), and nitric oxide (NO) confirmed by the liver histopathological alterations. The mechanistic inflammatory expression of inducible nitric oxide synthase (iNOS) and nuclear factor-kappa B (NF-ĸB), and expression of caspase-3 protein prominently increased. Zinc supplementation significantly modulated serum liver function markers, antioxidant enzymes, and GSH and MDA levels. Zinc downregulated the expression of cytokines, NO, iNOS, NF-ĸB and caspase-3, and ameliorated histopathological changes. Zinc protects against TAM-induced hepatotoxicity; it may serve as an adjuvant supplement for female patients undergoing TAM chemotherapy.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"115 - 123"},"PeriodicalIF":3.2,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1669243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43215844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Hasnat, Ziqiao Yuan, Aftab Ullah, M. Naveed, F. Raza, Mirza Muhammad Faran Ashraf Baig, Asifullah Khan, Dengqiu Xu, Yuwen Su, Linxin Sun, Luyong Zhang, Zhenzhou Jiang
{"title":"Mitochondria-dependent apoptosis in triptolide-induced hepatotoxicity is associated with the Drp1 activation","authors":"M. Hasnat, Ziqiao Yuan, Aftab Ullah, M. Naveed, F. Raza, Mirza Muhammad Faran Ashraf Baig, Asifullah Khan, Dengqiu Xu, Yuwen Su, Linxin Sun, Luyong Zhang, Zhenzhou Jiang","doi":"10.1080/15376516.2019.1669247","DOIUrl":"https://doi.org/10.1080/15376516.2019.1669247","url":null,"abstract":"Abstract How triptolide is associated with mitochondrial dysfunction and apoptosis in connection with its hepatotoxicity remains unclear. The objective of our study was to find out the link between mitochondrial dynamics and cell death in triptolide induced hepatotoxicity. We treated L02 cells with 25 nM concentration of triptolide. The results demonstrated that triptolide treatment caused an increase in apoptotic cell death, mitochondrial depolarization, ROS overproduction, a decrease in ATP production, and mitochondrial fragmentation which in turn is associated with the activation of Drp1 fission protein. Triptolide treatment led to the translocation of Drp1 from the cytosol into outer mitochondrial membrane where it started mitochondrial fission. This fission event is coupled with the mitochondrial release of cytochrome c into the cytosol and subsequently caspase-3 activation. TEM analysis of rat liver tissues revealed the distortion of mitochondrial morphology in triptolide-treated group. Western blot analysis explained that disruption in mitochondrial morphology was attached with the recruitment of Drp1 to mitochondria, cytochrome c release, and caspase-3 activation. However, Mdivi-1 co-treatment inhibited the activation of Drp1 and caspase-3 and blocked the release of cytochrome c into the cytosol. In short, inhibiting Drp1 protein activation may provide a new potential target for curing Drp1-associated apoptosis in triptolide-induced hepatotoxicity.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"124 - 133"},"PeriodicalIF":3.2,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1669247","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47206962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Validation and kinetic of enzymatic method for the detection of organophosphate insecticides based on cholinesterase inhibition","authors":"S. Badawy","doi":"10.1080/15376516.2019.1669248","DOIUrl":"https://doi.org/10.1080/15376516.2019.1669248","url":null,"abstract":"Abstract Kinetic and validation of the enzymatic method for the determination of fenitrothion organophosphorus based on cholinesterase inhibition were studied. A Linear relationship was obtained with a determination coefficient R2 of 0.9989 suggesting that the noncompetitive inhibition kinetic equation is suitable to represent the enzymatic assay of fenitrothion. The value of the inhibition constant KI was 0.374 mg/ml/min. The analytical logarithmic curve for the determination of fenitrothion concentration using the percentage of cholinesterase inhibition presented good linear relations at concentrations of 0.05–2 mg/ml (R2 = 0.9889). The maximum inhibition 83% was observed at 2.0 mg/ml final assay concentration. The lower inhibition 3.3% was observed at 0.05 mg/ml detection limit. The experimental measurement condition was optimized. The enzymatic method exhibited detection limits (LOD) in the range of 0.05–2.0 mg/ml. The limit of quantification (LOQ) was 0.06 mg/ml with inhibition 13%. The concentration of fenitrothion that inhibited the hydrolysis of substrate by 50% (IC50 value) was 0.4 mg/ml. Standard deviations and coefficients of variation indicate a good precision of the enzymatic method for the detection of organophosphate insecticides at an incubation time of 20 min.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"134 - 138"},"PeriodicalIF":3.2,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1669248","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45420705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yuanyuan Zhang, C. Kong, Huimin Chi, Junxia Li, Jie Xing, Fei Wang, Lijun Shao, Qingfeng Zhai
{"title":"Effect of a beta-cypermethrin and emamectin benzoate pesticide mixture on reproductive toxicity in male mice in a greenhouse environment","authors":"Yuanyuan Zhang, C. Kong, Huimin Chi, Junxia Li, Jie Xing, Fei Wang, Lijun Shao, Qingfeng Zhai","doi":"10.1080/15376516.2019.1669241","DOIUrl":"https://doi.org/10.1080/15376516.2019.1669241","url":null,"abstract":"Abstract With the widespread use of pesticides, the resistance to pesticides of pests has gradually increased, caused mixed pesticides to become even more widely used for practical applications. To investigate the effects of mixed pesticides on reproductive health in an occupational greenhouse environment, the greenhouse environment and the characteristics of the actual application were constructed, and then the male mice were comprehensively exposed to a mixture of the beta-cypermethrin and emamectin benzoate environmental. Additionally, the effect of the beta-cypermethrin and emamectin benzoate mixture on the reproductive health of male mice was known. The results showed that with the prolongation of exposure duration, the activities of Glutathione Peroxidase (GSH-Px), Total Superoxide Dismutase (T-SOD), Lactate dehydrogenase (LDH) and Acid phosphatase (ACP) in the testes of mice gradually decreased and the activity of Malondialdehyde (MDA) gradually increased. It was also found that the apoptosis rate of murine testicular cells increased and that DNA damage occurred with prolonged exposure duration. Therefore, it can be inferred that exposure to a mixture of the pesticides beta-cypermethrin and emamectin benzoate in the greenhouse environment may have adverse effects on the reproductive health of male mice.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"100 - 106"},"PeriodicalIF":3.2,"publicationDate":"2020-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1669241","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48189815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Alavi, A. Shamsizadeh, G. Karimi, A. Roohbakhsh
{"title":"Transient receptor potential ankyrin 1 (TRPA1)-mediated toxicity: friend or foe?","authors":"M. Alavi, A. Shamsizadeh, G. Karimi, A. Roohbakhsh","doi":"10.1080/15376516.2019.1652872","DOIUrl":"https://doi.org/10.1080/15376516.2019.1652872","url":null,"abstract":"Abstract Transient receptor potential (TRP) channels have been widely studied during the last decade. New studies uncover new features and potential applications for these channels. TRPA1 has a huge distribution all over the human body and has been reported to be involved in different physiological and pathological conditions including cold, pain, and damage sensation. Considering its role, many studies have been devoted to evaluating the role of this channel in the initiation and progression of different toxicities. Accordingly, we reviewed the most recent studies and divided the role of TRPA1 in toxicology into the following sections: neurotoxicity, cardiotoxicity, dermatotoxicity, and pulmonary toxicity. Acetaminophen, heavy metals, tear gases, various chemotherapeutic agents, acrolein, wood smoke particulate materials, particulate air pollution materials, diesel exhaust particles, cigarette smoke extracts, air born irritants, sulfur mustard, and plasticizers are selected compounds and materials with toxic effects that are, at least in part, mediated by TRPA1. Considering the high safety of TRPA1 antagonists and their efficacy to resolve selected toxic or adverse drug reactions, the future of these drugs looks promising.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"1 - 18"},"PeriodicalIF":3.2,"publicationDate":"2020-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1652872","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44152423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Biao Zhang, P. Wei, J. Men, Shuman Zhang, H. Shao, Zhihu Zhang
{"title":"Crotonaldehyde-induced alterations in testicular enzyme function and hormone levels, and apoptosis in the testes of male Wistar rats are associated with oxidative damage","authors":"Biao Zhang, P. Wei, J. Men, Shuman Zhang, H. Shao, Zhihu Zhang","doi":"10.1080/15376516.2019.1646369","DOIUrl":"https://doi.org/10.1080/15376516.2019.1646369","url":null,"abstract":"Abstract Crotonaldehyde is a hazardous pollutant present in cigarette smoke and automobile exhausts that is generated by lipid peroxidation, and harmful to reproductive organs. Although we are often exposed to low doses of crotonaldehyde daily, its adverse effects on the reproductive organs have not been fully elucidated. To elucidate them, we administered crotonaldehyde (0, 2.5, 4.5, and 8.5 mg/kg) by gavage for 150 days to male Wister rats, and evaluated its effect on their testicular tissues. Body weight, testis coefficient, sperm count, and motility decreased. Reactive oxygen species and malondialdehyde levels in the 8.5 and 4.5 mg/kg groups significantly increased as antioxidant enzyme activity decreased. Testicular cell apoptosis rate in the exposed groups increased. Testicular enzyme activity and reproductive hormone levels were significantly altered in the 8.5 and 4.5 mg/kg groups. Therefore, long-term exposure to crotonaldehyde may induce oxidative stress, resulting in testicular cell apoptosis, and testicular enzyme and hormone level alteration.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"19 - 32"},"PeriodicalIF":3.2,"publicationDate":"2020-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1646369","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43342545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. O. Heck, V. A. Zborowski, P. M. Chagas, S. D. da Luz, C. F. Bortolatto
{"title":"p-Chloro-diphenyl diselenide attenuates plasma lipid profile changes and hepatotoxicity induced by nonionic surfactant tyloxapol in rats","authors":"S. O. Heck, V. A. Zborowski, P. M. Chagas, S. D. da Luz, C. F. Bortolatto","doi":"10.1080/15376516.2019.1669240","DOIUrl":"https://doi.org/10.1080/15376516.2019.1669240","url":null,"abstract":"Abstract Tyloxapol is a nonionic surfactant oligomer inductor of dyslipidemia, which in turn is a risk factor for liver damage. Selenium-based compounds have emerged as promising therapeutic candidates for treating different experimental disorders. This study investigated the effects of p-chloro-diphenyl diselenide (p-ClPhSe)2 on toxicity induced by Tyloxapol in rats. Plasma lipid profile, hepatic functionality and oxidative stress parameters were evaluated in adult male Wistar rats treated with (p-ClPhSe)2 (10 mg/kg; oral administration by gavage) for seven days and exposed to a single Tyloxapol injection (400 mg/kg; intraperitoneal route) 30 min after the last (p-ClPhSe)2 treatment. Tyloxapol exposure increased the plasma levels of total cholesterol, triacylglycerol, non-HDL-cholesterol and the calculated cardiac risk index (CRI). The plasma activities of alanine and aspartate aminotransferase (ALT and AST, liver function markers) were increased in rats exposed to Tyloxapol, which demonstrates a hepatic lipotoxicity. In the liver, reactive oxygen species (ROS) content was enhanced and the non-protein sulfhydryl (NPSH) levels were decreased by Tyloxapol. The data revealed that repeated treatment with (p-ClPhSe)2 reduced plasma lipid alterations and hepatotoxicity induced by Tyloxapol. Although (p-ClPhSe)2 did not reduce ROS levels increased by Tyloxapol, it increased NPSH content in the liver. Pearson’s correlation coefficient revealed a positive relationship between the levels of hepatic NPSH and plasma HDL. HDL is known by eliciting antioxidant activity; therefore, the improvement in HDL function could be suggested as a therapeutic target. In conclusion, the results demonstrate the protective effects of (p-ClPhSe)2 on the hepatic lipotoxicity induced by Tyloxapol in rats.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"73 - 80"},"PeriodicalIF":3.2,"publicationDate":"2020-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1669240","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46064656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Exposure of BPA and its alternatives like BPB, BPF, and BPS impair subsequent reproductive potentials in adult female Sprague Dawley rats","authors":"Saman Ijaz, Asad Ullah, G. Shaheen, S. Jahan","doi":"10.1080/15376516.2019.1652873","DOIUrl":"https://doi.org/10.1080/15376516.2019.1652873","url":null,"abstract":"Abstract Bisphenol A (BPA) and its alternatives are extensively used in household and industrial products. BPA and its alternatives have affinity for estrogen receptors and mimic its actions. The present study aims to examine the comparative effects of BPA and its alternatives bisphenol B (BPB), bisphenol F (BPF), and bisphenol S (BPS) on the reproductive health in adult female rats. One hundred and seventy post-weaning female rats (90 ± 25) were divided into 17 groups and assigned for different treatments. Control and treated groups were injected with concentrations of 50–500 µg/ml and 5–50 mg/kg of BPA, BPB, BPF, and BPS for 28 days. The results showed adverse morphological and histopathological alterations in rat ovaries in all treated groups. A remarkable decrease was observed in antral and corpus luteum follicles while rise in atretic and cystic follicles in the ovaries of BPA and its alternatives 5 and 50 mg/kg treated groups when compared with control. Significant decrease in catalase (CAT), super oxidase (SOD), and peroxidase (POD) levels was noted while increase in the values of thiobarbituric acid reactive substance (T-BARS) and reactive oxygen species (ROS) was observed when BPA and its alternatives groups were compared with the control. Hormones were also observed with alterations in their concentrations when treated groups were compared with the control. The current data suggest that BPA and its alternatives exposure during the pre-pubertal stage have the potential to induce oxidative stress and histopathological changes during follicular development in female rats.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"60 - 72"},"PeriodicalIF":3.2,"publicationDate":"2020-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1652873","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49623604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The effects of heavy metals on human metabolism","authors":"Zhushan Fu, Shuhua Xi","doi":"10.1080/15376516.2019.1701594","DOIUrl":"https://doi.org/10.1080/15376516.2019.1701594","url":null,"abstract":"Abstract As technology continues to advance, heavy metals in drinking water have exceeded recommended limits from regulators around the world. The main source of human exposure to heavy metals is from contaminated drinking water. The effects of drinking water contaminated with heavy metals, such as arsenic, lead, nickel, cadmium and mercury, have gradually caught the attention of the relevant departments and personnel. It is well known that occupational exposure to heavy metals occurs as a result of using these metals in a variety of industrial processes in and/or a variety of materials, including color pigments and alloys. A series of adverse effects on human metabolism has resulted from exposure to heavy metal-contaminated drinking water, which has been recorded from around the world. The general mechanism of heavy metal toxicity is through the production of reactive oxygen species, the appearance of oxidative damage, and subsequent adverse effects on health. Therefore, water contaminated with heavy metals causes high morbidity and mortality worldwide. In order to address concern regarding the health effects of different heavy metals, this paper reviews its sources, distribution and effects of heavy metal on human metabolism. HIGHLIGHTS The accumulation of heavy metals such as lead, arsenic, mercury, cadmium and nickel will destroy the main metabolic process of human body. Redox reactions in biological systems are caused by carcinogenic metal ions such as nickel and arsenic. The free radicals produced by these reactions cause oxidative damage to proteins and DNA. The accumulation of heavy metals eventually produces reactive oxygen species that can cause oxidative stress, which may lead to the production of various diseases.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"167 - 176"},"PeriodicalIF":3.2,"publicationDate":"2019-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1701594","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44667703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Latifa Knani, M. Venditti, Safa Kechiche, M. Banni, I. Messaoudi, S. Minucci
{"title":"Melatonin protects bone against cadmium-induced toxicity via activation of Wnt/β-catenin signaling pathway","authors":"Latifa Knani, M. Venditti, Safa Kechiche, M. Banni, I. Messaoudi, S. Minucci","doi":"10.1080/15376516.2019.1701595","DOIUrl":"https://doi.org/10.1080/15376516.2019.1701595","url":null,"abstract":"Abstract Among heavy metals, cadmium (Cd) is one of the most toxic for health due to it accumulation in several tissues including bone. Since melatonin (MLT) favors new bone formation through several pathways including Wnt/β-catenin, here we assessed whether MLT has a protective role against Cd induced toxicity in the rat bone tissue. Adult male Wistar rats receiving 50 mg CdCl2/L and/or 3 mg/L MLT were used and were sacrificed 30 days after the treatment. Femurs and plasma were collected and analyzed by various biochemicals, molecular and histological investigation. The results showed that Cd exposure induced bone disorder characterized by histopathological alterations, a decreased alkaline phosphatase activity and plasmatic concentration of osteocalcin. Moreover, also the expression levels of some osteogenic-related genes (Runx2, Ocn and Alp) were down-regulated after Cd treatment. Since mechanistically Cd toxicity reduced the Kinase activity of GSK3β and protein levels of Wnt3a and β-catenin, we observed that MLT administration significantly ameliorated the toxic effects induced by the metal. Our findings provide clues about a potential protective effect of MLT against Cd-induced bone metabolism destruction and that the protection was partially mediated via the Wnt/β-catenin signaling pathway.","PeriodicalId":49117,"journal":{"name":"Toxicology Mechanisms and Methods","volume":"30 1","pages":"237 - 245"},"PeriodicalIF":3.2,"publicationDate":"2019-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/15376516.2019.1701595","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43494886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}